We conducted a systematic review of all studies published between 1950 and 2007 of associations between long-term exposure to ambient air pollution and the risks in adults of nonaccidental mortality and the incidence and mortality from cancer and cardiovascular and respiratory diseases. We searched bibliographic databases for cohort and case-control studies, abstracted characteristics of their design and conduct, and synthesized the quantitative findings in tabular and graphic form. We assessed heterogeneity, estimated pooled effects for specific pollutants, and conducted sensitivity analyses according to selected characteristics of the studies. Our analysis showed that long-term exposure to PM2.5 increases the risk of nonaccidental mortality by 6% per a 10 microg/m3 increase, independent of age, gender, and geographic region. Exposure to PM2.5 was also associated with an increased risk of mortality from lung cancer (range: 15% to 21% per a 10 microg/m3 increase) and total cardiovascular mortality (range: 12% to 14% per a 10 microg/m3 increase). In addition, living close to busy traffic appears to be associated with elevated risks of these three outcomes. Suggestive evidence was found that exposure to PM2.5 is positively associated with mortality from coronary heart diseases and exposure to SO2 increases mortality from lung cancer. For the other pollutants and health outcomes, the data were insufficient data to make solid conclusions.

A systematic review of the relation between long-term exposure to ambient air pollution and chronic diseases.

Environmental carcinogens, in a strict sense, include outdoor and indoor air pollutants, as well as soil and drinking water contaminants. An increased risk of mesothelioma has consistently been detected among individuals experiencing residential exposure to asbestos, whereas results for lung cancer are less consistent. At least 14 good-quality studies have investigated lung cancer risk from outdoor air pollution based on measurement of specific agents. Their results tend to show an increased risk in the categories at highest exposure, with relative risks in the range 1.5-2.0, which is not attributable to confounders. Results for other cancers are sparse. A causal association has been established between exposure to environmental tobacco smoke and lung cancer, with a relative risk in the order of 1.2. Radon is another carcinogen present in indoor air which may be responsible for 1% of all lung cancers. In several Asian populations, an increased risk of lung cancer is present in women from indoor pollution from cooking and heating. There is strong evidence of an increased risk of bladder, skin and lung cancers following consumption of water with high arsenic contamination; results for other drinking water contaminants, including chlorination by-products, are inconclusive. A precise quantification of the burden of human cancer attributable to environmental exposure is problematic. However, despite the relatively small relative risks of cancer following exposure to environmental carcinogens, the number of cases that might be caused, assuming a causal relationship, is relatively large, as a result of the high prevalence of exposure.

/pdf/contribution-of-environmental-factors-to-cancer-risk-3n6zyq13ie.pdf

Contribution of environmental factors to cancer risk

Smoking is a known lung cancer cause, but no detailed quantitative systematic review exists. We summarize evidence for various indices. Papers published before 2000 describing epidemiological studies involving 100+ lung cancer cases were obtained from Medline and other sources. Studies were classified as principal, or subsidiary where cases overlapped with principal studies. Data were extracted on design, exposures, histological types and confounder adjustment. RRs/ORs and 95% CIs were extracted for ever, current and ex smoking of cigarettes, pipes and cigars and indices of cigarette type and dose–response. Meta-analyses and meta-regressions investigated how relationships varied by study and RR characteristics, mainly for outcomes exactly or closely equivalent to all lung cancer, squamous cell carcinoma (“squamous”) and adenocarcinoma (“adeno”). 287 studies (20 subsidiary) were identified. Although RR estimates were markedly heterogeneous, the meta-analyses demonstrated a relationship of smoking with lung cancer risk, clearly seen for ever smoking (random-effects RR 5.50, CI 5.07-5.96) current smoking (8.43, 7.63-9.31), ex smoking (4.30, 3.93-4.71) and pipe/cigar only smoking (2.92, 2.38-3.57). It was stronger for squamous (current smoking RR 16.91, 13.14-21.76) than adeno (4.21, 3.32-5.34), and evident in both sexes (RRs somewhat higher in males), all continents (RRs highest for North America and lowest for Asia, particularly China), and both study types (RRs higher for prospective studies). Relationships were somewhat stronger in later starting and larger studies. RR estimates were similar in cigarette only and mixed smokers, and similar in smokers of pipes/cigars only, pipes only and cigars only. Exceptionally no increase in adeno risk was seen for pipe/cigar only smokers (0.93, 0.62-1.40). RRs were unrelated to mentholation, and higher for non-filter and handrolled cigarettes. RRs increased with amount smoked, duration, earlier starting age, tar level and fraction smoked and decreased with time quit. Relationships were strongest for small and squamous cell, intermediate for large cell and weakest for adenocarcinoma. Covariate-adjustment little affected RR estimates. The association of lung cancer with smoking is strong, evident for all lung cancer types, dose-related and insensitive to covariate-adjustment. This emphasises the causal nature of the relationship. Our results quantify the relationships more precisely than previously.

/pdf/systematic-review-with-meta-analysis-of-the-epidemiological-szurlrfmky.pdf

Systematic review with meta-analysis of the epidemiological evidence in the 1900s relating smoking to lung cancer

Epidemiological studies on the effect of urban air pollution on lung cancer were surveyed. Overall, the studies from many countries point to a smoking-adjusted risk in urban areas over countryside areas that is higher by a factor of up to 1.5. The extent to which urban air pollution contributes to this excess remains unknown. Studies on diesel-exposed occupational groups show that urban air pollution may have a causative role in lung cancer. Model calculations on unit risk factors of known human carcinogens were carried out to rank carcinogens according to their current ambient air concentrations.

Cancer risk of air pollution: epidemiological evidence.

Environmental carcinogens, in a strict sense, include outdoor and indoor air pollutants, as well as soil and drinking water contaminants. An increased risk of mesothelioma has consistently been detected among individuals experiencing residential exposure to asbestos, while results for lung cancer are less consistent. Several good-quality studies have investigated lung cancer risk from outdoor air pollution based on measurement of specific agents. Their results tend to show an increased risk in the categories at highest exposure, with relative risks in the range 1.5. A causal association has been established between exposure to environmental tobacco smoke and lung cancer, with a relative risk in the order of 1.2. Radon is another carcinogen present in indoor air, with a relative risk in the order of 1.06 for exposure at 100 Bq/m3. In several Asian populations, an increased risk of lung cancer results among women from indoor pollution from cooking and heating. There is strong evidence of an increased risk of bladder, skin and lung cancers following consumption of water with high arsenic contamination; results for other drinking water contaminants, including chlorination by-products, are inconclusive. A total of 29 occupational agents are established human carcinogens, and another 30 agents are suspected carcinogens. In addition, at least 12 exposure circumstances entail exposure to carcinogens. Exposure is still widespread for many important occupational carcinogens, such as asbestos, coal tar, arsenic and silica, in particular in developing countries. Although estimates of the global burden of occupational and environmental cancer result in figures in the order of 2% and less than 1%, respectively, these cancers concentrate in subgroups of the population; furthermore, exposure is involuntary and can, to a large extent, be avoided.

/pdf/epidemiology-of-environmental-and-occupational-cancer-1wnnxljgqt.pdf

Epidemiology of environmental and occupational cancer.

American Legion members from throughout California were surveyed via questionnaire. Lung cancer mortality for L.A. was no greater than for other urban areas. The relative risk gradient from smoking was less than in other studies. Age-adjusted mortality rate from lung cancer for nonsmokers, 1/2 pack, 1 pack, and > 1 pack smokers living in San Francisco Bay area, San Diego, or other mixed urban-rural counties was 44 and 11, 77 and 61, 135 and 125, and 226 and 138 (per 100,000 man-years), respectively. For those groups living in L.A., the rate was 28, 64, 126, and 241, respectively.

Cancer of the lung and Los-Angeles-type air pollution

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Cancer of the lung and Los-Angeles-type air pollution